Evidence map›Paper›PMID 27470005›Full record

ArticleJournal of autoimmunity2016

IDO-orchestrated crosstalk between pDCs and Tregs inhibits autoimmunity.

Carla Lippens, Fernanda V Duraes, Juan Dubrot, Dale Brighouse, Mathilde Lacroix, Magali Irla, Jean-Pierre Aubry-Lachainaye, Walter Reith, Judith N Mandl, Stéphanie Hugues

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of autoimmunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
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  4. Frontiers in cellular neuroscience · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 2 countries.

Carla LippensDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Fernanda V DuraesDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Juan DubrotDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Dale BrighouseDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Mathilde LacroixDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Magali IrlaDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Jean-Pierre Aubry-LachainayeFlow Cytometry Core Facility, University of Geneva, 1211 Geneva 4, Switzerland.
Walter ReithDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland.
Judith N MandlLymphocyte Biology Section, Laboratory of Systems Biology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Stéphanie HuguesDepartment of Pathology and Immunology, University of Geneva, 1211 Geneva 4, Switzerland. Electronic address: stephanie.hugues@unige.ch.
University of Geneva · CHNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Plasmacytoid dendritic cells (pDCs) have been shown to both mediate and prevent autoimmunity, and the regulation of their immunogenic versus tolerogenic functions remains incompletely understood. Here we demonstrate that, compared to other cells, pDCs are the major expressors of Indoleamine-2,3-dioxygenase (IDO) in steady-state lymph nodes (LNs). IDO expression by LN pDCs was closely dependent on MHCII-mediated, antigen-dependent, interactions with Treg. We further established that IDO production by pDCs was necessary to confer suppressive function to Tregs. During EAE development, IDO expression by pDCs was required for the generation of Tregs capable of dampening the priming of encephalitogenic T cell and disease severity. Thus, we describe a novel crosstalk between pDCs and Tregs: Tregs shape tolerogenic functions of pDCs prior to inflammation, such that pDCs in turn, promote Treg suppressive functions during autoimmunity.

Indexed as

AnimalsAutoimmunityCells, CulturedCoculture TechniquesDendritic CellsEncephalomyelitis, Autoimmune, ExperimentalFlow CytometryGene Expression Regulation, EnzymologicHistocompatibility Antigens Class IIHumansIndoleamine-Pyrrole 2,3,-DioxygenaseLymph NodesMice, Inbred C57BLMice, TransgenicReverse Transcriptase Polymerase Chain ReactionT-Lymphocytes, RegulatoryHistocompatibility Antigens Class IIIndoleamine-Pyrrole 2,3,-DioxygenaseAntigen presentationExperimental autoimmune encephalomyelitisIndoleamine 2,3-dyoxygenasePlasmacytoid dendritic cellsRegulatory T cellsTolerance

Identifiers

PMID27470005
PMCPMC5127883
OpenAlexW2494934438

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.